Nrf2 contributes to the weight gain of mice during space travel.
Takafumi SuzukiAkira UrunoAkane YumotoKeiko TaguchiMikiko SuzukiNobuhiko HaradaRie RyokeEriko NaganumaNanae OsanaiAya GotoHiromi SudaRyan BrowneAkihito OtsukiFumiki KatsuokaMichael ZorziTakahiro YamazakiDaisuke SaigusaSeizo KoshibaTakashi NakamuraSatoshi FukumotoHironobu IkehataKeizo NishikawaNorio SuzukiIkuo HiranoRitsuko ShimizuTetsuya OishiHozumi MotohashiHirona TsubouchiRisa OkadaTakashi KudoMichihiko ShimomuraThomas W KenslerHiroyasu MizunoMasaki ShirakawaSatoru TakahashiDai ShibaMasayuki YamamotoPublished in: Communications biology (2020)
Space flight produces an extreme environment with unique stressors, but little is known about how our body responds to these stresses. While there are many intractable limitations for in-flight space research, some can be overcome by utilizing gene knockout-disease model mice. Here, we report how deletion of Nrf2, a master regulator of stress defense pathways, affects the health of mice transported for a stay in the International Space Station (ISS). After 31 days in the ISS, all flight mice returned safely to Earth. Transcriptome and metabolome analyses revealed that the stresses of space travel evoked ageing-like changes of plasma metabolites and activated the Nrf2 signaling pathway. Especially, Nrf2 was found to be important for maintaining homeostasis of white adipose tissues. This study opens approaches for future space research utilizing murine gene knockout-disease models, and provides insights into mitigating space-induced stresses that limit the further exploration of space by humans.
Keyphrases
- oxidative stress
- weight gain
- signaling pathway
- high fat diet induced
- gene expression
- genome wide
- body mass index
- metabolic syndrome
- public health
- copy number
- type diabetes
- single cell
- birth weight
- ms ms
- risk assessment
- physical activity
- endothelial cells
- social media
- heat stress
- pi k akt
- health promotion
- gestational age